SARS-CoV-2 infection and increasing autoimmune disorders among ICU-hospitalized COVID-19 patients.

In acute conditions, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes multi-organ damage due to the induction of inappropriate immune responses, particularly lung tissue fibrosis. To evaluate the consequence of the deterioration of the immune system, autoimmune markers were assessed. In a case-control study, 108 patients with coronavirus disease 2019 (COVID-19) were admitted to the intensive care unit (ICU), and 158 outpatients with mild clinical symptoms, with SARS-CoV-2 reverse transcription quantitative polymerase chain reaction (RT-qPCR) positive tests, were included for comparison. The demographic and hematologic variables and presence of the main autoantibodies in sera of 40 eligible ICU-hospitalized COVID-19 patients and 40 COVID-19 outpatients were assessed. Out of 108 COVID-19 ICU-hospitalized patients, 40 were selected as the control group (40/158) who had no underlying diseases before hospitalization, according to their self-declaration and clinical records at the time of admission. The results demonstrated that the main complete blood count indices, such as red blood cells and platelets, decreased dramatically in ICU-hospitalized patients. Furthermore, the autoantibody profiles were positive in 45% and 15% of ICU-admitted patients for antinuclear antibodies and antineutrophilic cytoplasmic autoantibodies, respectively. In ICU patients, anti-PM/Scl 100 or AMA-M2 was 33%. Anti SS-A, anti-SS-B, anti-Ro-52, and anti-Jo-1 in 11.5% for each one were reactive. Other autoantibodies of the ICU group were as follows: CENP (5.6%), Rib-protein (5.6%), and nucleosome (5.6%). However, only two individuals in the control group had positive results for SS-A and SS-B (5%). Induction of such particular autoantibodies by the virus can justify the multi-organ involvement and severity of the disease in ICU patients, which may also cause other organ involvement in the long term.